Three Salmonella strains differ in virulence, we showed previously, because their lipopolysaccharide (LPS) activates complement differentially via the alternative pathway, resulting in different amounts of C3b on the bacteria, and thereafter different phagocytosis by macrophages. We find, using a system containing purified C3, B and D, that the generation of C3b depended on the structure of the LPS. As expected, the least virulent strain activates C3 the most, the most virulent does so the least. The degradation of bound C3b is LPS-independent. In other experiments, we used artificial short O-antigen polysaccharides (PS) and found that they also showed differential activation; thus only primary structure of PS and not structure of core sugars of lipid of LPS is required. Bacteria are somtimes killed and degraded by macrophages; factors influencing these processes are poorly understood. We find that certain bacterial molecules including LPS and certain proteins persist in macrophages even when easliy killed bacteria are ingested and will characterize these phenomena further. Many bacteria make LPS in two groups of lengths - one short and one much longer, the difference relecting different numbers of PS repeating units. We find that a mutant deprived of sugar required to make PS responds by continuing to make longer chains at a reduced rate, rather than shortening their length. We have measured both PS length distribution and sensitivity to agents that kill when they reach the membrane. Analysis by computer shows that slight increases in density of very long chains cause large decreases in the area and size of places where the killing agents could reach the membrane, so we postulate that the cell maximizes its protection by this method.